| Literature DB >> 24649036 |
Abstract
Hypoxic-ischemic encephalopathy (HIE) is an important cause of brain injury in the newborn and may result in long-term devastating consequences. Excessive stimulation of glutamate receptors (GluRs) is a pivotal mechanism underlying ischemia-induced selective and delayed neuronal death. Although initial studies focused on N-methyl-D-aspartic acid (NMDA) receptors as critical mediators in HIE, subsequent studies supported a more central role for α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (AMPARs), particularly Ca2+-permeable AMPARs, in brain damage associated with hypoxia-ischemia. This study reviewed the important role of Ca2+-permeable AMPARs in HIE and the future potential neuroprotective strategies associated with Ca2+-permeable AMPARs.Entities:
Keywords: Ca2+-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors; glutamate receptors 2; hypoxic-ischemic encephalopathy; neonate
Year: 2013 PMID: 24649036 PMCID: PMC3916971 DOI: 10.3892/br.2013.154
Source DB: PubMed Journal: Biomed Rep ISSN: 2049-9434